Evidence map›Paper›PMID 34642818›Full record

ReviewBasic research in cardiology2021

Regulation of STAT3 and its role in cardioprotection by conditioning: focus on non-genomic roles targeting mitochondrial function.

Stefano Comità, Saveria Femmino, Cecilia Thairi, Giuseppe Alloatti, Kerstin Boengler, Pasquale Pagliaro, Claudia Penna

Open access · hybridAbstract readReview
In one paragraph

Review in Basic research in cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
7.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 87 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Stefano ComitàDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, Orbassano, 10043, Torino, TO, Italy.
Saveria FemminoDepartment of Medical Sciences, University of Turin, Torino, Italy.
Cecilia ThairiDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, Orbassano, 10043, Torino, TO, Italy.
Giuseppe AlloattiUni-Astiss, Polo Universitario Rita Levi Montalcini, Asti, Italy.
Kerstin BoenglerInstitute of Physiology, University of Giessen, Giessen, Germany.
Pasquale PagliaroDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, Orbassano, 10043, Torino, TO, Italy. pasquale.pagliaro@unito.it.ORCID http://orcid.org/0000-0002-4386-1383
Claudia PennaDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, Orbassano, 10043, Torino, TO, Italy. claudia.penna@unito.it.
University of Turin · ITAzienda Sanitaria Locale di Asti · ITJustus-Liebig-Universität Gießen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia-reperfusion injury (IRI) is one of the biggest challenges for cardiovascular researchers given the huge death toll caused by myocardial ischemic disease. Cardioprotective conditioning strategies, namely pre- and post-conditioning maneuvers, represent the most important strategies for stimulating pro-survival pathways essential to preserve cardiac health. Conditioning maneuvers have proved to be fundamental for the knowledge of the molecular basis of both IRI and cardioprotection. Among this evidence, the importance of signal transducer and activator of transcription 3 (STAT3) emerged. STAT3 is not only a transcription factor but also exhibits non-genomic pro-survival functions preserving mitochondrial function from IRI. Indeed, STAT3 is emerging as an influencer of mitochondrial function to explain the cardioprotection phenomena. Studying cardioprotection, STAT3 proved to be crucial as an element of the survivor activating factor enhancement (SAFE) pathway, which converges on mitochondria and influences their function by cross-talking with other cardioprotective pathways. Clearly there are still some functional properties of STAT3 to be discovered. Therefore, in this review, we highlight the evidence that places STAT3 as a promoter of the metabolic network. In particular, we focus on the possible interactions of STAT3 with processes aimed at maintaining mitochondrial functions, including the regulation of the electron transport chain, the production of reactive oxygen species, the homeostasis of Ca

Indexed as

Myocardial Reperfusion InjurySTAT3 Transcription FactorHumansMitochondriaMitochondria, HeartReactive Oxygen SpeciesSignal TransductionReactive Oxygen SpeciesSTAT3 protein, humanSTAT3 Transcription FactorCa2+ regulationIschemia reperfusion injuryMitochondrial permeability transition poreReactive oxygen speciesRISK pathwaySAFE pathwaySTAT3STAT5

Identifiers

PMID34642818
PMCPMC8510947
OpenAlexW3206034954

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.